Changes in hunger neuron signaling may help to explain post-diet weight gain.
Researchers looked into the “yo-Yo effect,” which is often used to describe the neural processes that cause weight gain after dieting.
They discovered through mouse experiments that after a diet, brain cell signaling changes.
After these times of calorie restriction, they found that blocking a particular neural pathway resulted in less weight gain.
To see how these results apply to humans, more research is required.
The most popular way to lose weight is through diet. However, the majority of dieters who lose weight do so in the long run. This phenomenon is referred to as the “yo effect.”
Unknown are the precise mechanisms underlying the Yo-Yo effect. However, research indicates that the hypothalamus’ arcuate nucleus (ARC), a region of the brain, is crucial in controlling appetite and weight gain.
Additionally, research demonstrates that food restriction affects synaptic inputs to ARC neurons, which regulate body weight.
The creation of obesity treatments may benefit from additional investigation into how ARC neurons affect food intake and weight gain.
Recently, researchers looked into how ARC neurons are impacted by diet restriction, which in turn affects weight gain.
They discovered that in mice who die, weight gain is decreased by blocking the neural pathways that activate these ARC neurons.
Published in Cell MetabolismTrusted Source was the study.
Weight gain and ARC neurons
The study’s focus was on AgRP neuronsTrusted Source, an ARC neuron type that is closely related to hunger. According to studies, these neurons are activated when caloric intake is restricted, such as during fasting, which results in increased feeding and weight gain.
The post-mortem brains of mice were examined by the researchers to study these neurons. Prior to that, some mice had fasted for 16 hours.
Optogenetics, which uses light to activate cells, was then used by the researchers to stimulate AgRP neurons-related brain regions.
They discovered that compared to mice that did not fast, the paraventricular hypothalamic nucleus (PVH) of the mouse had more activity. Growth and metabolism are both influenced by PVH.
The fasted group, who were fed a calorically restricted diet for an additional 6 days after their fast, experienced this activation for several days, according to the researchers.
The next question was whether inhibiting PVH neurons could lower mice’s food intake. They did this by silencing these neurons in a different mouse group and monitoring their 24-hour fasting food intake.
They discovered that mice in a control group consumed about 33% less food than mice with inhibited PVH neurons. Over the following seven days, they also put on less weight.
Further tests revealed that mice’s amplified signaling from PVH neurons returned to normal once they regained the weight they had lost while fasting.
The goal of the research is to develop long-term weight loss therapies.
MNT discussed the study’s limitations with Dr. Mir Ali, a bariatric surgeon and medical director at Orange Coast Medical Center in Fountain Valley, California.
The hunger-satiety balance is a complex interaction of hormones and neural signals, and it may not be as easily applicable to humans, the study is about an animal model and is focused on one specific pathway, he said.
Medical News Today reported that Dr. Mark Guido, an endocrinologist with Novant Health Forsyth Endocrine Consultants in Winston Salem, North Carolina, was not a study participant.
Additionally, the study only demonstrates the existence of a neural pathway for weight regain, not the fact that humans can currently be definitively targeted with this information to aid in weight loss.
potential for fresh anti-obesity therapies
Dr. Ali responded: “When questioned about the study’s implications:
The findings have the implication that if a particular neural pathway can be identified to block the hunger signal, then an intervention or medication may be effective in preventing weight regain or even aiding in weight loss. It is obvious that much more research is required, particularly in regards to humans.
The results, according to Dr. Guido, strengthen the growing body of proof that weight is “more than a math problem” or that “calories in versus calories out” are important factors.
The majority of research now suggests that we should consider it a brain-related disorder and that our brain actively works to induce weight gain. Because of this, the majority of diet and exercise-only programs fail to result in significant long-term weight loss. To encourage weight regain, the brain can alter the equation in its favor.
Mark Guido, Dr.
The majority of our best weight-loss medications work in the brain, and thanks to this newer understanding, we are starting to treat obesity as a chronic disease with long-term medications targeted at the underlying body processes. He came to the conclusion that the discovery of this new pathway creates a fresh potential drug target.